...
首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Malt 1-dependent RelB cleavage promotes canonical NF-kB activation in lymphocytes and lymphoma cell lines
【24h】

Malt 1-dependent RelB cleavage promotes canonical NF-kB activation in lymphocytes and lymphoma cell lines

机译:麦芽1依赖RelB裂解促进淋巴细胞和淋巴瘤细胞系中的经典NF-kB激活

获取原文
获取原文并翻译 | 示例
           

摘要

The protease activity of the paracaspase Malti contributes to antigen receptor-mediated lymphocyte activation and lymphoma-genesis. Malti activity is required for optimal NF-kB activation, but little is known about the responsible substrate(s). Here we report that Malti cleaved the NF-kB family member RelB after Arg-85. RelB cleavage induced its proteasomal degradation and specifically controlled DNA binding of RelA- or c-Rel-containing NF-kB complexes. Overexpression of RelB inhibited expression of canonical NF-kB target genes and led to impaired survival of diffuse large B-cell lymphoma cell lines characterized by constitutive Malti activity. These findings identify a central role for Malti-dependent RelB cleavage in canonical NF-kB activation and thereby provide a rationale for the targeting of Malti in immunomodula-tion and cancer treatment.
机译:对半胱氨酸蛋白酶Malti的蛋白酶活性有助于抗原受体介导的淋巴细胞活化和淋巴瘤的产生。 Malti活性是获得最佳NF-kB激活所必需的,但对负责的底物了解甚少。在这里我们报告说,Malti在Arg-85之后裂解了NF-kB家族成员RelB。 RelB的切割诱导了其蛋白酶体降解,并特别控制了含有RelA或c-Rel的NF-kB复合物的DNA结合。 RelB的过表达抑制了规范性NF-kB靶基因的表达,并导致以组成性Malti活性为特征的弥漫性大B细胞淋巴瘤细胞系的存活受损。这些发现确定了Malti依赖的RelB裂解在经典NF-kB激活中的核心作用,从而为免疫调节和癌症治疗中Malti的靶向提供了理论依据。

著录项

  • 来源
  • 作者单位

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Hematology, Oncology and Tumor Immunology, Charite-Universitaetsmedizin Berlin, D-13353 Berlin, Germany;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

    Department of Physics, Philipps-University Marburg, D-35032 Marburg, Germany;

    Department of Hematology, Oncology and Tumor Immunology, Charite-Universitaetsmedizin Berlin, D-13353 Berlin, Germany;

    Department of Physics, Philipps-University Marburg, D-35032 Marburg, Germany;

    Department of Hematology, Oncology and Tumor Immunology, Charite-Universitaetsmedizin Berlin, D-13353 Berlin, Germany;

    Department of Biochemistry, University of Lausanne, CH-1066 Epalinges, Switzerland;

  • 收录信息 美国《科学引文索引》(SCI);美国《生物学医学文摘》(MEDLINE);美国《化学文摘》(CA);
  • 原文格式 PDF
  • 正文语种 eng
  • 中图分类
  • 关键词

    signal transduction; t-cell receptor;

    机译:信号转导;t细胞受体;

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号